Arsenic‐induced encephalopathy

Danan, Marc; Dally, S; Canso, F.

doi:10.1212/wnl.34.11.1524

Cited by 23 publications

(10 citation statements)

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“…Only a few studies have evaluated the effect of arsenic exposure on brain function. [18][19][20] Calderon et al 18 found that arsenic exposure is associated with lower verbal IQ and poorer longterm memory in children. The Agency for Toxic Substances and Disease Registry 17 has stated that acute toxic exposures to inorganic arsenic have been shown to lead to emotional lability and memory loss.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Chronic Diseases in Adults Exposed to Arsenic-Contaminated Drinking Water

2004

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Inorganic arsenic is naturally occurring in groundwaters throughout the United States. This study investigated arsenic exposure and self-report of 9 chronic diseases. We received private well-water samples and questionnaires from 1185 people who reported drinking their water for 20 or more years. Respondents with arsenic levels of 2 microg/L or greater were statistically more likely to report a history of depression, high blood pressure, circulatory problems, and bypass surgery than were respondents with arsenic concentrations less than 2 microg/L.

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Section: Discussionmentioning

confidence: 99%

Prevalence of Chronic Diseases in Adults Exposed to Arsenic-Contaminated Drinking Water

2004

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“…Patients may also exhibit central nervous system depression and cognitive dysfunction (hallucinations, delirium, decreased memory, and confusion). 15,16 Persistent QT c prolongation and the accompanying risk of torsades de pointes occur among patients with clinically significant body burdens of arsenic. 17 Aldrich-Mees lines, ie, whitish transverse discoloration of the nails resulting from temporary interruption of growth plate activity, may occur within 40 days after acute arsenic poisoning but are rarely seen, occurring for only 5% of patients.…”

Section: Subacute Toxicity (24 Hours To 4 Weeks)mentioning

confidence: 99%

Acute Arsenic Poisoning in Two Siblings

et al. 2005

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We report a case series of acute arsenic poisoning of 2 siblings, a 4-month-old male infant and his 2-year-old sister. Each child ingested solubilized inorganic arsenic from an outdated pesticide that was misidentified as spring water. The 4-month-old child ingested a dose of arsenic that was lethal despite extraordinary attempts at arsenic removal, including chelation therapy, extracorporeal membrane oxygenation, exchange transfusion, and hemodialysis. The 2-year-old fared well with conventional therapy.

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“…Arsenic is a chemical element in our living environment; however, overexposure of arsenics by contaminated food and water is known to induce systemic damage, including the peripheral and central nervous systems (CNS) [1][2][3][4][5]. An oxidative mechanism is reportedly involved in the arsenite-induced neurotoxicity [5][6][7][8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Melatonin Ameliorates Arsenite-Induced Neurotoxicity: Involvement of Autophagy and Mitochondria

Teng¹,

Tai²,

Huang

et al. 2015

Mol Neurobiol

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In the present study, the neuroprotective effect of melatonin on arsenite-induced neurotoxicity was investigated in rat primary cultured cortical neurons. Incubation of melatonin prevented arsenite-induced neuronal cell loss in a concentration-dependent manner. Furthermore, melatonin significantly attenuated arsenite-induced elevation in microtubule-associated protein light chain 3 (LC3)-II levels, a biomarker of autophagy. Our fluorescent staining assay showed that melatonin decreased arsenite-induced elevation of co-localized fluorescent puncta of monodansylcadaverine (a specific marker of autophagic vacuoles) and lysotracker red (a specific marker of lysosomes), indicating that melatonin is capable of inhibiting arsenite-induced autophagy and autolysosome formation. Because 3-methyladenine (an autophagic inhibitor) attenuated the arsenite-reduced α-synuclein levels (a protein essential for the neurite outgrowth and synaptic plasticity), melatonin via inhibiting autophagy attenuated the arsenite-reduced α-synuclein levels. At the same time, melatonin ameliorated the arsenite-induced reduction in growth associated protein 43 (a hallmark protein of neurite outgrowth) and discontinuous neurites of rat primary cultured cortical neurons. In addition, melatonin was found to prevent arsenite-induced decreases in cytochrome c oxidase levels (a biomarker of mitochondrial mass) and elevation in co-localized fluorescent puncta of autolysosomes and cytochrome c oxidase. Moreover, melatonin prevented arsenite-induced reduction in peroxisome proliferator-activated receptor gamma co-activator 1 α, a transcriptional co-activator of mitochondrial biosynthesis. Taken together, melatonin may exert its neuroprotective action via inhibiting arsenite-induced autophagy and enhancing mitochondrial biogenesis and thus restoring α-synuclein levels, neuronal integrity, and mitochondrial mass in rat primary cultured cortical neurons.

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Arsenic‐induced encephalopathy

Cited by 23 publications

References 0 publications

Prevalence of Chronic Diseases in Adults Exposed to Arsenic-Contaminated Drinking Water

Prevalence of Chronic Diseases in Adults Exposed to Arsenic-Contaminated Drinking Water

Acute Arsenic Poisoning in Two Siblings

Melatonin Ameliorates Arsenite-Induced Neurotoxicity: Involvement of Autophagy and Mitochondria

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